| Project/Area Number |
26461938
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Gunma University |
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Principal Investigator |
Fujii Takaaki 群馬大学, 医学部附属病院, 助教 (40507331)
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| Co-Investigator(Kenkyū-buntansha) |
茂木 晃 群馬大学, 大学院医学系研究科, 准教授 (10323362)
堤 荘一 群馬大学, 医学部附属病院, 講師 (30323356)
森田 廣樹 群馬大学, 医学部附属病院, 医員 (70646794)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 腫瘍血管新生 / リンパ節転移 / VEGF / リンパ節外浸潤 / エリブリン / TGF-β / PDGF-AA / mTOR / FDG-PET / 血管新生因子 / バイオマーカー / 脈管襲侵 / 抗腫瘍効果 |
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| Outline of Final Research Achievements |
We hypothesized that the mTOR inhibitor-induced anticancer effect is affected by expression of a key angiogenic factor, vascular endothelial growth factor (VEGF). The key observations made in this study can be summarized as follows: 1) administration of rapamycin dose-dependently reduced cell viability of MCF-7, but did not reduce cell viability of HT-29; 2) rapamycin reduced VEGF expression in the culture medium of MCF-7, while rapamycin did not contribute VEGF expression to the culture medium of HT-29; 3) VEGF stimulated cell viability and VEGF inhibition reduced cell viability of MCF-7; and 4) rapamycin dose-dependently restored the cell viability of MCF-7 reduced by rapamycin. These results demonstrate the critical role of VEGF in the action of rapamycin as an anticancer agent on MCF-7. We also revealed that lymph node metastasis and ECI suggest poor prognosis and, especially ECI represent lymphatic aggressive disease and also biological aggressiveness in cases with breast cancer.
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